Pulmonary Diseases PDF

Pulmonary Dysfunctions & Disorders N111 Pathopharmacology 1 Samuel Merritt University Structures of the Pulmonary System (cont’d) Pulmonary Circulation Systemic Tissues Alveolar cells Type I: epithelial structure cells Type II: produce surfactant Lowers surface t...

Pulmonary Dysfunctions & Disorders N111 Pathopharmacology 1 Samuel Merritt University Structures of the Pulmonary System (cont’d) Pulmonary Circulation Systemic Tissues Alveolar cells Type I: epithelial structure cells Type II: produce surfactant Lowers surface tension Facilitates gas exchange Immune function Alveolar macrophages- phagocytize foreign particles Damaged by smoking and silica Pulmonary and Bronchial Circulation Six Barrie rs Signs and Symptoms of Pulmonary Disease  Dyspnea  Subjective sensation of uncomfortable breathing  Orthopnea  Dyspnea when a person is lying down  Paroxysmal nocturnal dyspnea (PND)  Hemoptysis Hypoxemia Deficient blood oxygen  arterial O2  hemoglobin saturation Issue of ventilation & perfusion Gas Exchange Principles Ventilaton (VA) Perfusion (Q) VA:Q BEST: dependent lung fields Need to match adequate volume of air in the alveoli with adequate blood flow Best ventilation-perfusion ratio is 0.8 Ventilation-Perfusion Imbalances Underperfused Underventilated Underperfused alveoli: High  Adequate ventilation &  perfusion  Underperfusion Pulmonary emboli (PE) Systemic lupus erythematosus (SLE) Sarcoidosis Alveolar carcinoma Underventilated alveoli: Low Airways are partially obstructed   airflow rates  VA:Q O2 therapy Underventilation Causes: Atelectasis Pneumonia (PNA) Hypoxia Hypoxic Circulatory hypoxia hypoxia Low cardiac High altitude output Hypovent. shock Obstruction Histotoxic Anemic hypoxia hypoxia Cyanide low Hgb poisoning Shifting transport Oxygen (Oxyhemoglocin) dissociation curve  O2 affinity   release of O2 to tissues  Shift to the left  O2 affinity   release of O2 to Factors that shift the curve To the Left To the Right  pH  pH  PCO2  PCO2  temp  temp Hyperthryoidism Carboxyhemoglobin Anemia Hypothyroidism Chronic hypoxemia Bank blood COPD Congenital heart dz  Hyperventilation: Pathogenesis Increase air supply   CO2 removal  hypocapnia Hyperventilation: Etiologies Pain, fever Obstructive & restrictive lung diseases Brainstem injury Sepsis Anxiety High altitude Metabolic acidosis  Hypoventilation: Pathogenesis Insufficient air supply   O2 absorption &  CO2 removal  hypercapnia & hypoxemia  Hypoventilation: Etiologies Respiratory depression medications Opiates, barbiturates Myasthenia gravis Paralysis of respiratory muscles Guillain-Barre Syndrome Obesity Obstructive sleep apnea Chest wall damage Metabolic alkalosis Pulmonary Obstruction Lumen Loss of Bronchiectas Parenchyma is Emphysema Bronchiolitis (COPD Type A) † Cystic Wall of the Fibrosis Lumen Epiglottitis Asthma † Acute bronchitis Chronic Asthma Airway obstruction that is reversible  airway responsiveness to stimuli 5% to 12% of U.S. population Most common chronic disease of children Asthma Types Extrinsic Intrinsic Exercise-Induced Occupational asthma Extrinsic Asthma Pediatric onset Allergy related IgE mediated response common Involves histamine/leukotrienes Extrinsic Asthma: Pathogenesis Inflammatory factors Mast cell/eosinophil release vasoactive amines Cytokine cascade activation Cells: neutrophils, lymphocytes Edema Airway obstruction factors Acute bronchospasm Mucus production  Mucus plug formation CHRONIC: Airway wall remodeling: thickening of basement membrane Extrinsic Asthma Extrinsic Asthma: Pathogenesis Extrinsic Asthma: Pathogenesis Asthma: Clinical Manif. Wheezing-expiratory Feeling of tightness of chest Dyspnea Cough Increased sputum production Hyperinflated chest Decreased breath sounds Asthma: Treatment Imp. Severe Asthma Attack Use of accessory muscles of respiration Distant breath sounds with inspiratory wheezing Orthopnea Agitation Tachypnea > 30 breaths/min Tachycardia > 120 beats/min Status asthmaticus Status Asthmaticus: Treatment Imp. Epinephrine IV corticosteroids subcutaneous terbutaline oxygen therapy mechanical ventilation? COPD Type A Emphysema Pink puffer Type B Chronic bronchitis Blue bloater COPD A: Etiologies Smoking >70 packs/year Air pollution Certain occupations Mining Welding Asbestos α1-Antitrypsin deficiency COPD A: Pulmonary changes COPD A: Clinical Manifes. Thin, often frail appearance Progressive DOE/SOB Use of accessory muscles Pursed-lip breathing Diminished/absent cough Hypoxemia/hypercapnia Digital clubbing Barrel chest Cor pumonale Thin and frail Barrel Chest Clubbing/ pursed lip breathing COPD B: Etiologies Also known as chronic bronchitis Cigarette smoking (90%) Repeated airway infections Genetic predisposition Inhalation of physical or chemical irritants COPD B: Pathogenesis-2  Resistance to breathing  O2 demands Fibrosis Slow alveoli  empty/ fill Mucus Hypoxemia VQ mismatch  Bronchi al Hypercapnia thicknes s Destruction of Dilation of airway bronchial wall sacs/pus filled Chronic Obstructive Pulmonary Disease (cont’d) Obstructive Pulmonary Disease COPD: Treatment Goals Block the progression of the disease Return to optimal respiratory function Return to usual activities of daily living COPD: Medications Low-dose O2 therapy Inhaled short acting B2 agonists Inhaled bronchodilators Inhaled/oral corticosteroids Theophylline products Cough suppressants Antimicrobial agents COPD: Management Smoking cessation exposure of irritants Adequate rest Proper hydration Physical reconditioning Influenza and pneumococcal vaccines Restrictive: Pleural Space Disorders Pneumothorax † Pleural Effusion † Pleural Space Disorders Pneumothor Air ax trapped Pus/ Pleural Effusion fluid trapped  Pneumothorax: E & P Secondary pneumothorax Result of complications from preexisting pulmonary disease May be due to rupture of cyst or bleb  Pneumothorax: E & P Spontaneous (primary) pneumothorax Tall, thin males, 20-40 years old Cigarette smoke increases risk Rupture Air small Rib cage enters Lung subpleur springs pleural collapses al blebs out space in apices  Pneumothorax: Etiology Tension pneumothorax Trauma  Non/penetrating injury May be iatrogenic  Tension Pneumothorax: Pathogenesis Air enters pleural space during inspiration Cannot escape during expiration Ipsilateral lung collapse Contralateral mediastinal shift  Venous return &  Cardiac output Pneumothorax  Pleural Effusion: Types 5 major types Transudates (low in protein)  hydrostatic or  oncotic pressure Associated with severe heart failure or other edematous states Exudates (High in protein) Causes: malignancies, infections, PE, sarcoidosis, post-MI syndrome  Pleural Effusion: Types Empyema High-protein exudative effusion Infection in the pleural space Hemothorax Presence of blood in pleural space Result of chest trauma Contains blood and pleural fluid Chylothorax or lymphatic Exudative process that develops from trauma Pleural Effusion: Pathogenesis Intrapleur Pleural capillary Colloid al hydrostatic press. oncotic pressure ∆s pressure ∆s ∆s  Fluid  Fluid removal gathered in from pleural pleural space space  Permeability of Impaired pleural lymphatic membrane drainage Exudate collection  Pleural Effusion: Clinical Manif. Asymptomatic